کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8287170 | 1535838 | 2017 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Butyrate induces ROS-mediated apoptosis by modulating miR-22/SIRT-1 pathway in hepatic cancer cells
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کلمات کلیدی
ECLABTSDIOC6HDACGPXNAC2′,7′-dichlorodihydrofluorescein diacetate - 2 '، 7'-dichlorodihydrofluorescein diacetateDMSO - DMSOROS - ROSenhanced chemiluminescence - بهبود شیمیایی لومنnon-alcoholic fatty liver disease - بیماری کبدی چربی غیر الکلیTUNEL - تونلCell proliferation - تکثیر سلولیApoptosis - خزان یاختهایDimethyl sulfoxide - دیمتیل سولفواکسیدShort chain fatty acid - زنجیره کوتاه اسید چربSOD - سدSuperoxide dismutase - سوکسوکس دیسموتازN-acetyl cysteine - نیتستیل سیستئینhistone deacetylase - هیستون داستیلازHepatocellular carcinoma - کارسینوم هپاتوسلولار(کارسینوم سلولهای استخوانی)glutathione peroxidase - گلوتاتیون پراکسیدازReactive oxygen species - گونههای فعال اکسیژن3,3′-dihexyloxacarbocyanine iodide - یدید 3،3'-dihexyloxacarbocyanine
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
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چکیده انگلیسی
Butyrate is one of the short chain fatty acids, produced by the gut microbiota during anaerobic fermentation of dietary fibres. It has been shown that it can inhibit tumor progression via suppressing histone deacetylase and can induce apoptosis in cancer cells. However, the comprehensive pathway by which butyrate mediates apoptosis and growth arrest in cancer cells still remains unclear. In this study, the role of miR-22 in butyrate-mediated ROS release and induction of apoptosis was determined in hepatic cells. Intracellular expression of miR-22 was increased when the Huh 7 cells were incubated with sodium butyrate. Over-expression of miR-22 or addition of sodium butyrate inhibited SIRT-1 expression and enhanced the ROS production. Incubation of cells with anti-miR-22 reversed the effects of butyrate. Butyrate induced apoptosis via ROS production, cytochrome c release and activation of caspase-3, whereas addition of N-acetyl cysteine or anti-miR-22 reversed these butyrate-induced effects. Furthermore, sodium butyrate inhibited cell growth and proliferation, whereas anti-miR-22 inhibited these butyrate-mediated changes. The expression of PTEN and gsk-3 was found to be increased while p-akt and β-catenin expression was decreased significantly by butyrate. These data showed that butyrate modulated both apoptosis and proliferation via miR-22 expression in hepatic cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Redox Biology - Volume 12, August 2017, Pages 340-349
Journal: Redox Biology - Volume 12, August 2017, Pages 340-349
نویسندگان
Kishor Pant, Ajay K. Yadav, Parul Gupta, Rakibul Islam, Anoop Saraya, Senthil K. Venugopal,